RESUMO
The structure of the A1 gene of Zea mays was determined by sequencing cDNA and genomic clones. The gene is composed of four exons and three short introns. The 40.1-kd A1 protein is an NADPH-dependent reductase. Germinal derivatives of the mutable a1-m1 allele with either recessive or wild-type phenotype have been isolated. Sequence analysis of these revertant alleles indicates that frame-shift mutations abolish A1 gene function, whereas one additional amino acid within the protein sequence still allows wild-type gene expression. The presence of a second, promoter-like structure, upstream of the functional A1 gene promoter is discussed with respect to its possible involvement in differential expression of the A1 gene. The structure of the a1-m2 8004, 3456 and 4412 alleles, featuring distinguishable phenotypes in the presence of Spm(En), was also determined. In all alleles the 1080-bp-long inhibitor (I) element is located 15 bp upstream of the CAAT box of the A1 gene promoter. The unusual response of a1-m2 alleles to trans-active signals of the Spm(En) element is discussed with respect to the position of the I inserts. Also presented are data on the structure and insertion sites of transposable elements determined by cloning and sequencing of the mutable a1 alleles a1-mpapu, a1-mr 102 and a1-ml.
Assuntos
Oxirredutases do Álcool/genética , Elementos de DNA Transponíveis/genética , Genes de Plantas/genética , Proteínas de Plantas/genética , Zea mays/genética , Alelos , Sequência de Bases , Dados de Sequência Molecular , FenótipoRESUMO
Two states of the a1-m1 allele featuring different phenotypes in the absence as well as in the presence of Spm or En have been cloned and sequenced.. The insertion site and orientation of the Inhibitor (I) element within the two alleles is identical. The sizes of the I elements differ, being 2.2 kb in state 6078 and 789 bp in state 5719A-1. The internal deletion in state 5719A-1 affects sequences within one side of the terminal inverted repeats of the I element. This alteration can be correlated with the decreased response of this state to the Mutator function of Spm. A model for the interaction between Spm (En)-encoded functions and the receptor element is discussed explaining the phenotypic differences between the states of the locus.
